Step 1 - Pharm - Antiarrhythmics (1Staid)

Front 1

These are the class IA antiarrhythmics

Back 1

Quinidine, procainamide, disopyramide
"The Queen Proclaims Diso's pyramid"

Front 2

These are the class IB antiarrhythmics

Back 2

Lidocaine, mexiletine, tocainide
"Lidy's Mexican Tacos"

Front 3

These are the class IC antiarrhythmics

Back 3

Flecainide, encainide, propafenon

Front 4

These are the class II antiarrhythmics

Back 4

Propranolol, esmolol, metoprolol, atenolol, timolol

Front 5

These are the class III antiarrhythmics

Back 5

Sotalol, ibutilide, amiodarone
(K-channel blockers. Amiodarone also has some beta-blocking activity)

Front 6

These are the class IV antiarrhythmics

Back 6

Verapamil, diltiazem

Front 7

These are other antiarrhythmics

Back 7

Adenosine, digoxin, potassium, magnesium

Front 8

These antiarrhythmics are contraindicated in post-MI patients because they are proarrhythmic

Back 8

Class IC (flecainide, encainide, propafenone)

Front 9

What effect does hyperkalemia have on class I drugs?

Back 9

Increases toxicity
(increased potassium means more Na channel blocking activity can take place, since these drugs are use-dependent)

Front 10

What effects do class IA drugs have?

Back 10

Increase AP duration, increase refractory period, increase QT interval, thereby slowing the heart down
(same as class III)

Front 11

These drugs affect both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia

Back 11

Class IA (quinidine, procainamide, disopyramide)
They affect Na channels thus have more impact on myocardium than nodes

Front 12

What effect do class IB drugs have?

Back 12

Decrease AP duration

Front 13

These drugs affect ischemic or depolarized Purkinje and ventricular tissue

Back 13

Class IB drugs (lidocaine, mexiletine, tocainide)

Front 14

These drugs are useful in acute ventricular arrhythmia
(which tend to have slower rhythms)

Back 14

Class IB drugs (lidocaine, mexiletine, tocainide), which decrease the AP duration and therefore speed up HR

Front 15

These drugs are useful in digitalis-induced arrhythmia

Back 15

Class IB drugs (lidocaine, mexiletine, tocainide)

Front 16

These drugs have no effect on AP duration

Back 16

Class IC (flecainide, encainide, propafenone)

Front 17

These drugs cannot be used in patients with cardiac structural abnormalities

Back 17

Class IC (flecainide, encainide, propafenone)

Front 18

These drugs significantly prolong refractory period in AV node

Back 18

Class IC (flecainide, encainide, propafenone)

Front 19

Increasing the AP duration has these other effects (as seen in class IA drugs)

Back 19

Increasing the AP duration also increases the refractory period and the QT interval

Front 20

These drugs increase the PR interval

Back 20

Class II (beta blockers) and class IV (calcium channel blockers). Increased PR interval corresponds with AV node suppression

Front 21

These drugs are used to decrease ventricular firing rate during atrial fibrillation and atrial flutter

Back 21

Class II (propranolol, esmolol, metoprolol, atenolol, timolol)

Front 22

These drugs may mask the signs of hypoglycemia

Back 22

Class II (propranolol, esmolol, metoprolol, atenolol, timolol)

Front 23

This drug can cause dyslipidemia

Back 23

Metoprolol

Front 24

What effects do class III drugs have?

Back 24

Increase AP duration, increase refractory period, increase QT interval--i.e., they slow the heart down
(same as class IA)

Front 25

What is the danger of sotalol?

Back 25

Progression to torsades de pointes

Front 26

What is the danger of bretylium?

Back 26

New arrhythmia, hypotension

Front 27

What is the danger of amiodarone?

Back 27

Pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism; also corneal deposits, skin deposits resulting in photodermatitis, constipation, CV effects (bradycardia, heart block, CHF)

Front 28

Check PFTs, LFTs and thyroid function tests (TFTs) when using this drug

Back 28

Amiodarone

Front 29

What affects do calcium channel blockers have?

Back 29

Decrease conduction velocity, increase refractory period, increase PR interval

Front 30

These drugs primarily affect AV nodal cells

Back 30

Calcium channel blockers (verapamil, diltiazem)

Front 31

These drugs are used in the prevention of nodal arrhythmias such as supraventricular tachycardia

Back 31

Calcium channel blockers (verapamil, diltiazem)

Front 32

Side effects of calcium channel blockers

Back 32

Flushing, edema, constipation, CV effects (CHF, AV block, sinus node depression)

Front 33

What is the drug of choice in diagnosing/abolishing AV nodal arrhythmias?

Back 33

Adenosine

Front 34

Side effects of adenosine

Back 34

Flushing, chest pain, hypotension

Front 35

MoA of adenosine

Back 35

Gets K out of the cells, thereby hyperpolarizing the cell and decreasing Ca release/contractility

Front 36

This is given to depress ectopic pacemakers as in digoxin toxicity

Back 36

Potassium. Given in hypokalemia

Front 37

This is given to treat torsades de pointes and digoxin toxicity

Back 37

Magnesium